• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Acetyl L- Glutathione, ATP, Baking Soda, Sam-e & Catalase = No PEM after exercise

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
Have you ever had an EBT Scan on your heart, which is a very low radiation version of a CAT scan? They can do calcium scoring to show the number of calcifications in your arterial system, all completely non invasive.
A problem with EBT is that not all plaque is calcified. In fact, calcification might even be protective insofar as stabilizing plaques. Most AMI happens not with the advanced, calcified and complicated plaques but with plaques at roughly only 30-50% stenosis (and with little to no plaque) that are unstable and therefore more likely to rupture or erode.

The price you quoted seems appealing, though. I've heard the rationale from a radiologist about the Late Gadolinium Enhancement MRI being best of all, but that's likely much much more expensive.
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
re: Thedoharides' MC stabilizer approach

MD researcher and clinician Theoharides uses his luteolin formula (and other flavonoids) to combat interstitial cystitis

https://duckduckgo.com/html/?q=theoharides interstitial cystitis

Here is his site: http://mastcellmaster.com/documents/Interstitial-Cystitis/Urology-IC-Immunomodulators-review.pdf reviewing pharm approaches.

He has a few good video interviews, too.

Thanks, but I don't get it any more, and I don't think it was interstitial cystitis anyway. I have been taking cranberry juice tablets every day for years now, which seems to keep it at bay.
 

pemone

Senior Member
Messages
448
Do you have evidence for nitrate intake increasing physiological nitric oxide levels?

I test it directly from my own body in realtime using the berkeleytest.com strips.

The chemistry of all of this is quite interesting. You eat nitrates. The body absorbs those and they come out in your saliva. Bacteria in the mouth then convert those to nitrites! You swallow the nitrites and *this* is what provides the substrate for nitric oxide! The test strips measure nitrites, not nitrates, so unless you are doing the conversion in your mouth the strips won't light up. Here is a fascinating overview of that process:

I can tell you there is no placebo effect here. I feel the effects to well being, to circulation, and to sexual health in very dramatic ways. It is not like being 20 again, but in terms of circulation feels like being in your 30s for sure.

I have only been eating the nitrate rich foods for about a month now. Arginine, Citrulline, and Neo40 all failed to do anything for my nitric oxide levels. It definitely has not cured my CFS, but I might also need to give it time and it might promote some good healing processes in the body that just take time.

I will read the NO threads later, thanks for the pointer.
 

pemone

Senior Member
Messages
448
A problem with EBT is that not all plaque is calcified. In fact, calcification might even be protective insofar as stabilizing plaques. Most AMI happens not with the advanced, calcified and complicated plaques but with plaques at roughly only 30-50% stenosis (and with little to no plaque) that are unstable and therefore more likely to rupture or erode.

The price you quoted seems appealing, though. I've heard the rationale from a radiologist about the Late Gadolinium Enhancement MRI being best of all, but that's likely much much more expensive.

I understand your point about non-calcified plaques being the most dangerous. But the point is that a person with a large number of plaques will have calcifications on *some* of those. Therefore the presence of calcifications becomes a marker that will make you aware of the problem. If you show zero calcifications, then don't you think it is highly unlikely that you would have a large number of uncalcified plaques?
 

pemone

Senior Member
Messages
448
Certainly I feel a bit better when taking the supplement vinpocetine, which is a cerebral vasodilator. ME/CFS patients in general have reduced blood flow to the brain.

Hip, you feel better when taking a known cerebral vasodilator. Your hands are cold all the time. You start to feel neurological symptoms when you eat foods that are known to lower bloodflow. It all paints a very consistent picture doesn't it? Your body is sending a really clear message.

I think you are exactly the guy for whom restoring nitric oxide *might* have a dramatic good result.


Sounds interesting. Although I don't have the general symptoms of arteriosclerosis, and can run a mile without problem (I don't get much physical PEM from my ME/CFS).

What are your primary exhaustion symptoms and what brings those on? What other symptoms make you think this is CFS? To me the hallmark of true CFS is the PEM. PEM on exertion is to me all about the mitochondria shouting for help. The body is in glycolysis. The electron transport chain is highly inefficient. The acidity in muscle tissue builds up and paralyzes muscle. The acidity becomes systemic and causes neurologic symptoms.


Very interesting. And those nitric oxide test strips from berkeleytest.com are quite inexpensive: you can buy 10 strips for $13.

I buy three 50 packs, and they had a "buy two get one free" deal recently.

After you learn how to eat, I don't think you will need to test as often. But it is a very tricky thing. I am finding that I can eat the three cups of celery in morning together with other foods in a blended shake and I don't get the same effect. It's going to take months before I really understand this. The strips are essential. I would not understand how to eat without them.

When you used these test strips, did you see changes in your saliva NO level after eating high nitrate foods?

The strips test nitrites, the precursor to nitric oxide. NO is too short lived to be worth testing. It is released in bursts as others have described. Yes, I go from zero nitrites to target range nitrites about 60 to 90 minutes after eating LARGE amounts of nitrate rich foods.

Though in spite of this short half life, there is a stable basal level of NO in the blood, because NO attaches to the albumin in the blood, to form S-nitroso-albumin, which acts as a carrier for NO.

I would love to understand it all better. I only get the nitrites to target levels for less than six hours of the day. Hopefully during those six hours enzymes and other metabolites are storing them to then use when nitrites go low. Since we don't have direct measurement of those other metabolites I cannot say.

It was quite a few years ago that I bought it, and I cannot remember where, but I notice that if you search eBay for sodium carbonate food grade you gets several hits.

I wouldn't trust small vendors selling a chemical like this and calling it "food grade". Some of that stuff will be from China, loaded with heavy metals, and I don't believe for a second that the manufacturer really tested the product widely. One manufacturer might source from 10 different vendors and not test every one of those.
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
I understand your point about non-calcified plaques being the most dangerous. But the point is that a person with a large number of plaques will have calcifications on *some* of those. Therefore the presence of calcifications becomes a marker that will make you aware of the problem. If you show zero calcifications, then don't you think it is highly unlikely that you would have a large number of uncalcified plaques?
Not to be argumentative, but I'd guess that only the opposite is true: if one finds cardiac calcium then one probably has intracranial calcium, too - which I think was your main point. But OTOH if one has zero calcium, then that likely means only that the exaggerated inflammatory response which produces calcification is missing. (AFAIK, calcification is a step beyond fibrosis, and fibroblasts can turn into osteoblasts in severe inflammation. That can also occur in lymph nodes, though it's rare there.)

Also, it's been known e.g. that carotid atheroma is not a surefire proxy for cardiac atheroma, so the underlying process/environment is somewhat different in different locations anyway.

Also, the overused cardiac catheterization can see only occlusion, yet the patient might still be at great risk of AMI because as you likely know the plaque begins its growth by pushing outward against the artery wall rather than bulging inward. Only an IVUS (Intra Vascular Ultra Sound) would spot that. IIRC Tij Russert had a good cath picture.. or was it a good treadmill test? ekg

As regards what you are saying to @Hip, maybe a CIMT (Carotid Intima Media Thickness) would be a better proxy for cerebral occlusion. But you had brought up age and if he is only around 30 yrs then I'd think that one would first look for an Fx of early onset problems.

pone, have you had an LDL-P or APO-B done?

Hey this is fun - I get to brush up on cardiac diagnostics :)
 
Last edited:

pemone

Senior Member
Messages
448
Once I read you should not brush your teeth in this period in order to get the NO, is it true?

That's what they say, yes, but I have not tested.

Also, there must be good mouthwash products that will minimize impact to the target bacteria, but I have not investigated.
 
Messages
5
The potassium ion is not intrinsically alkaline (nor intrinsically acidic for that matter). The pH depends what potassium is attached to; it depends on the whole molecule. For example, potassium bitartrate in a saturated solution has an acidic pH of around 3.5 (see here).

My apologies for being late to the conversation. But I have been asked by a member to clarify this point.

I have two contexts to add to this idea. First, the chemical pH context, and second, the metabolic acidity and alkalinity context.

First, both the cation and anion of a salt create pH effects. Each has differential affinity for the hydroxide part of water and the proton part of water. Water spontaneously dissociates into (hydrated) hydroxide and protons, and any selective interaction with one over the other creates pH shifts. So potassium (versus sodium, lithium, rubidium and cesium) does have differential effects on water pH. But since such "alkali" ions are so dramatically unreactive, their solitary effects are very subtle compared to the myriad of complex organic molecules that can be "decorated" with anionic (negatively charged) groups (e.g., carboxylic acid, ketone, aldehyde, ester) and cationic (positively charged) groups (e.g., alcohol, amine, ammonium, ether). So it is natural and practical to focus on the conspicuous and dismiss the subtle.

Second, the terms acid, acidifying and alkaline, alkalinizing have a non-chemical meaning in the context of biological systems and metabolism. This is popularized by the macrobiotic classifications of foods, nutrients, substances and drugs into acid-forming and alkaline-forming categories. These categorizations were made based on traditional Eastern medical principles that other people can describe. But independently, Dr. Emanuel Revici derived a similar classification almost 100 years ago by exposing rodents to various foods, nutrients, substances and drugs and measuring their resulting wound pH shifts with pH meters. There is a 85% congruence between these two lists. East meets west.

Revici's "archaic" terminology for this (homotrophic, heterotrophic) was "translated" as acidic and alkaline, but this is not the same acid and alkalinity of chemical pHs, despite being measured by such methods. His terminology has also be translated as catabolic and anabolic, and as aerobic and anaerobic, respectively. None of these translations is fully in accord with the modern uses of such terms. But since saying potassium is alkalinizing-anaerobic-anabolic in metabolic character and calcium is acidifying-aerobic-catabolic in character is quite awkward, it is simply described as alkaline, or anabolic, or anaerobic, with some kind of mutual understanding that this is a shorthand for the metabolic/biological meaning of the words.

If you want to know the chemistry and physics, the metabolic character of compounds turns out to be highly related to their charge when dissolved in water, their oxidative state and their electronic configuration. These do relate somewhat to pH, but it is also distinctly separate (as I understand it). When aerobic-acidifying-catabolic carboxylic acids and aldehydes are dissolved in water, they end up carrying a negative charge. In the case of carboxylic acids, it is substantial, and with aldehydes it is less. Catabolic elements (calcium, magnesium, copper, oxygen, sulfur, selenium) are electronically paired (they have an even humber of electrons in their outer orbitals. And the more oxidized organic structures are, the more likely they are catabolic-acidifying-aerobic. Alcohols and amines are reduced structures (fully loaded with hydrogen or hydride), carry positive charge when dissolved in water and are alkalinizing-anaerobic-anabolic in character. Among fatty acids, which are all acidic-aerobic-catabolic in character due to their carboxylic acid group, the higher oxidized PUFAs (polyunsaturated fatty acids) are among the most powerful catabolic-aerobic-acidifying structures that Revici ever quantified. Saturated fats are dramatically less acidifying. The structurally related fatty alcohols are very alkalinizing.

Experientially, there is no connection between the acidic or alkaline taste of a food or substance and its acid or alkaline metabolic effect. Lemon juice is very acidic (tart) on the tongue, but is substantially alkaline-anabolic-anaerobic in its metabolic effect. Sea vegetables (seaweeds) are powerfully alkalinizing-anaerobic-anabolic without having any conspicuous pH-associated taste.

Since I am new to this forum, I'd like any clarification from members as to whether this discussion is best kept as part of this thread or should be handled in a different manner. It is my considered opinion that this particular dimension of metabolism is highly relevant to autoimmune diseases and chronic fatigue states. But I also realize that it is highly complicated and is often counterintuitive in nature.

Advice and questions are welcome.
 
Messages
5
I have read that "ash" concept in various places too, but it is not really a scientific explanation.

It is scientific. (1) It is defined: the residue left over after combustion. (2) It is measurable: pH effects in urine, blood, tissue, cells and organelles (the latter two are exceedingly difficult). (3) It has been measured and found to be consistent. In other words, its predictions have been tested. (4) It has been systematized, and resulting predictions tested. (5) It has been applied practically, and clinically, with considerable success.

It is true that "ash" is not widely used by scientists in this field (biologists, physiologists, biophysicists) nor taught to physicians in medical school or in continuing medical education courses. But to the extent that I have discussed the issue with many scientists and alternative medical practitioners, the vast majority do readily understand the concept even if they do not have an intuitive or practical appreciation of it. I think it is important to note that the popularity of an scientific understanding or theory is political and temporal in nature and only tangentially related to the accepted meaning of "scientific."

In my opinion, it is not even relevant to "science." What scientists do (and do not do) does not define science.

In analogy: what religions do (and do not do) does not define spirituality, and what artists do (and do not do) does not define art.

The question I would ask you, and other members of this forum, is "is this understanding applicable to your health and wellbeing?"

Is there "medicine" (therapeutics in its broadest sense) that is useful to you that is also beyond the current practice of today's physicians? Is there not more to be learned and discovered about CFS and autoimmune conditions? And cannot the members of this group share information about their experiences with foods, supplements, herbs and diets constructively, to better help each other "figure out" how to better cope? A grass-roots think tank, if you will. Along with the creation of community and the fostering of emotional support, isn't what this site is about?

If such questions are deemed divisive and inappropriate by moderators or followers of this thread, might this be accommodated by creating a separate thread where such purposes can be chosen by those who want such foci?

I hope this is taken in the spirit in which it is offered.
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
Is there "medicine" (therapeutics in its broadest sense) that is useful to you that is also beyond the current practice of today's physicians? Is there not more to be learned and discovered about CFS and autoimmune conditions? And cannot the members of this group share information about their experiences with foods, supplements, herbs and diets constructively, to better help each other "figure out" how to better cope? A grass-roots think tank, if you will. Along with the creation of community and the fostering of emotional support, isn't what this site is about?

If such questions are deemed divisive and inappropriate by moderators or followers of this thread, might this be accommodated by creating a separate thread where such purposes can be chosen by those who want such foci?

I hope this is taken in the spirit in which it is offered.
Hi, Steve. Welcome and thanks for dropping in. I remember your name from your old CERI site from 20 years or so ago, a yellow background comes to mind. Since this is New Year's Eve, I'll also mention remembering you had a hangover preventive recipe. Lots of people here with CFS/ME can no longer tolerate alcohol since getting ill. As for myself, I seem to have always had a very high capacity to generate acetaldehyde dehydrogenase so I never did get the intolerance - though I haven't had any alcohol for a long time, just having no interest in it lately.

I also happen to think that exercise intolerance (aka PEM) here might be very related to exercise metabolites like malondiadehyde and the same lack in many people of aldehyde dehydrogenases. I overcame excercise intolerance years ago, by using... exercise.

I hope that you stick round for a while. It's interesting that you have been thinking about acidity and autoimmunity. The oxidized PUFA seems interesting.

P.S. I wouldn't worry about threads and OT and all that. Or any minor squabbling :) Please feel free to start any threads or make any comment anywhere that you want.

Happy New Year to you, Steve.
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
Advice and questions are welcome.
Steve, I personally notice acidic urine most after taking whey protein drinks (say 20-40 g). I know that some (not all?) amino acids are acidifying. But am I noticing the increased acidity because the AAs that I drink are going directly to the bladder? (That would be quite a waste.) Or do I get the acidity because the AAs that I drink quickly replace damaged proteins (glycation, oxidation, nitrosation) in myocytes or wherever - and it's those damaged AAs that cause my increased urine acidity?

Also, are oxidized proteins (which can't be repaired and are therefore excreted) more damaging on the way out than undamaged proteins? I'm comparing this to your comment on oxidized PUFA. Just by asking the question, I'm wondering if the whey should only be taken in small doses - in the setting of CFS.
 
Messages
5
Hi, Steve. Welcome and thanks for dropping in. I remember your name from your old CERI site from 20 years or so ago, a yellow background comes to mind. Since this is New Year's Eve, I'll also mention remembering you had a hangover preventive recipe. Lots of people here with CFS/ME can no longer tolerate alcohol since getting ill.

The "alcohol detox" formula was designed to handle aldehyde toxicity, specifically acetaldehyde from the first step in the alcohol metabolic pathway. It is spectacularly successful. The latest report I received from an engaged asian-extraction man being taken on a multi-day "bachelor's party" in Las Vegas was pretty impressive. He had a genetic problem with alcohol that had become worsened by age, and did not want to do the Vegas-alcohol "thing" with his buddies. But he blackmailed them into using the alcohol-detox formula with him. He was almost free of any alcohol toxicity during the excursion, and his buddies couldn't stop talking about it after the trip. He is now happily married, and still has his buddies as friends.

But there are several things that might be different with CFS/ME people beyond the classic chemical sensitivity to aldehydes. For example, the active ingredient in the formula is sulfur amino acids (cysteine and NAC), which are mild excitotoxic agents like glutamate (MSG), aspartate (frequently used as a mineral chelator in supplements), and aspartame (Nutrasweet, the artificial sweetener). It has been my observation that CFS and autoimmune-challenged individuals almost always have a low excitotoxic threshold and tend to react more readily to "Chinese restaurant syndrome." Some of this relates to B6 and magnesium deficiency, but I also think it is associated with lowered metabolic rate. And CFS and autoimmune people tend to run cold. Because I was taking excitotoxicity into consideration when formulating the supplement, I used low amounts of cysteine (50 mg) and NAC (50 mg) in each capsule. I added small amounts of all the B-complex vitamins, too. But the directions for use specify one capsule with each drink, and one when stopping drinking, so the total dose of cysteine+NAC could reach 500 mg on a binge, which is a dose that can produce excitotoxic reactions in sensitive people. Although it is spread out over time, that might not be enough to prevent excitotoxicity.

The aspect of this topic that relates to the topic thread re metabolic acid and alkaline is that alcohol is very much alkaline-anaerobic-anabolic in character, and it is spectacularly effective at suppressing ketosis (fat-burning) pathways. It also produces NADH from both alcohol dehydrogenase and acetaldehyde dehydrogenase. If a particular person is already over-reduced and has low levels of NAD+ and NADP+, drinking alcohol could make this much worse. So I am concerned that these efffects can produce "ripples" in the cellular/mitochondrial energy pathways similar to what happens in alcoholics, who experience a "high" when NADH rises and a "crash" when NADH falls. So as long as they keep drinking, and fresh alcohol keeps the NADH "propped up," they postpone the crash. This "biochemical imperative" to keep drinking is the difference between social drinkers and alcoholic addiction.

The alcohol formula is significantly acidifying-catabolic-aerobic due to the 100 mg of sulfur amino acids. This adds an alkaline-acid balance to the potential benefits and problems that might occur. If somebody with CFS is reacting to the alkalinizing effects of alcohol because they are already too alkaline, the acidifying effects of the formula could be balancing. But that could be a big assumption.

The time course of acid-alkaline shifts may not coincide with the acetaldehyde exposure. Many people have tried many different dosing protocols, like taking the alcohol-detox formula only before drinking, or only after drinking. But it seems to work decidedly better if the dosing brackets the alcohol ingestion (i.e., before AND after). This might not be the optimal dosing protocol for the acid-alkaline interactions.

I advise caution, attention and deliberation.
 
Messages
5
I also happen to think that exercise intolerance (aka PEM) here might be very related to exercise metabolites like malondiadehyde and the same lack in many people of aldehyde dehydrogenases. I overcame excercise intolerance years ago, by using... exercise.

Aldehydes as a class are problematic. They are cross-linking agents and biochemically reactive. So they could definitely be part of the post-exertion experience. However, I suspect that lactic acidosis from use of anaerobic energy pathways is probably the greater influence. It makes sense that exercise itself can ameliorate that, if it is mild enough to cause only minor lactic acid loading of tissues, and is increased slowly enough to induce constructive adaptation. But I am not convinced that this is likely to work in everybody because of different bottlenecks in aerobic metabolism that can cause a low aerobic threshold and reliance on anaerobic metabolism. Would exercise reverse loss of control of mercury? Would exercise reverse the T4-to-rT3 pathway? Would exercise improve redox control so that inflammation would be gradually lessened? And if there is metabolic entrainment, would exercise break it?
 
Messages
5
Steve, I personally notice acidic urine most after taking whey protein drinks (say 20-40 g). I know that some (not all?) amino acids are acidifying. But am I noticing the increased acidity because the AAs that I drink are going directly to the bladder? (That would be quite a waste.) Or do I get the acidity because the AAs that I drink quickly replace damaged proteins (glycation, oxidation, nitrosation) in myocytes or wherever - and it's those damaged AAs that cause my increased urine acidity?

Good questions. You are becoming a systems-level metabolic sleuther.

Sulfur amino acids are acidifying, and often show this at the blood-pH level, which is defended by the kidneys, so it shows up in the urine. Whey is rich in a cysteine dipeptide which is closely related to the glutathione tripeptide. So it is definitely acid-aerobic-catabolic. But the effect is not necessarily strong. So you are wise to as the secondary questions that go to other mechanisms of urine acidity.

The biggest and most rapid acidifier of urine is inflammation/allergy. I knew a woman with migraines who used her allergy to corn to successfully treat her migraine attacks. The early (prodromal) state for migraines is alkaline-anaerobic-anabolic stress, which shows in non-inflammed individuals as an alkaline trend in the urine which reaches an alkaline threshold (a different pH reading in each individual), at which time prostaglandins are produced to quickly acidify the body/blood stream and produce the full-blown migraine symptoms. By doing urine pH studies of herself, this woman figured out what this prodromal state "felt like." She would then eat a kernel of popped corn (or two) immediately after the first sign of a migraine coming on. The allergic reaction to the corn would acidify her body/blood quickly enough to abort the alkaline crisis and the impending migraine. This was successful roughly 90% of the time.

Popped corn is also highly acidic-catabolic-aerobic, in itself. Relatively high amounts of heat-damaged PUFAs. PUFAS are intrinsically acid-catabolic-aerobic, and rancid/oxidized PUFAs are doubly so.

I do not know why your urine acidifies like it does. There could be more involved than the simple acidification from sulfur amino acids (cysteine and methionine). You could be allergic to whey. Your gut microbiome could be shifting and producing acids, mycotoxins or allergens. There could be something else in your smoothie to which you are reacting.

Acid amino acids are also acidifying-aerobic-catabolic: glutamic acid and aspartic acid.

Fatty acids and fats (triglycerides) are also acidifying. PUFAs most of all. Do you put flax in your drink?

In a healthy individual, urine pH should regularly vary by 2 full pH units every 24 hours. That means a daytime pH of roughly 5 (4.5 to 5.5) and a some-time-during-the-night pH of roughly 7 (6.5 to 7.5). That's a hundredfold change in kidney excretion of protons. This pattern is highly circadian, being most acidic during the bulk of the day and most alkaline during the deep-sleep parts of the night.

In night owls, the pattern tends to be significantly delayed. Night owls often wake up with alkaline urine and usually show acid urine right up until they go to bed. Their urine acidity is slow to develop, just like their mental focus and physical performance. Ask a night-owl spouse to exercise in the AM and risk a divorce.

In morning larks, the pattern is advanced in time. Larks tend to wake up with acid urine, or have acid urine for their second urination (after voiding the pH-blended urine that accumulated during the night). And they often show urine alkalinization in the evening before going to bed.

A jet-lag pattern (acid at night and alkaline during the day) is often associated with chronic fatigue, intractable sleep problems and chronic brain fog.
 

Sherlock

Boswellia for lungs and MC stabllizing
Messages
1,287
Location
k8518704 USA
A jet-lag pattern (acid at night and alkaline during the day) is often associated with chronic fatigue, intractable sleep problems and chronic brain fog.
Steve, I could ask a dozen questions but don't want to overdo it. So here is just one for now. I see that I've failed to be brief, so just reading the bolded words below is good enough:

I've never seen that jet-lag pattern in acidity mentioned before. Now I realize that I mostly fit that. I used to be very much a night owl in the hours I kept before getting sick. I also have overactive mast cells, so histamine (the wakefulness chemical) is a big problem - once I awake because of the bladder, it is very hard to get back to sleep.

My bladder wakes me at ~200ml. Or with less volume, if there is a lot of acidity. (Or with strong spices before bed - but that one's easy to correct.) Or with much less bladder volume, for reasons I haven't identified yet. awry (NSAIDS or flavonoids like tart cherry) usually help - now thanks to you I understand why. Potassium citrate usually helps me delay the bladder wake-up-call. Exercise usually helps me sleep longer.

Melatonin 30g does nothing. The typical talk of sleep hygiene is to me like attacking a Sherman tank with a styrofoam cup.

My question: what else besides K citrate and anti-inflammatories could you recommend to reduce urine output - within the backdrop of pH or anything else? (I'm excluding prescription meds like desmopressin.)

Okay, a quick followup question if you don't mind: from what you know of polyuria in CFS, would it be wrong to try and reduce urine output? In other words, is the system getting rid of excess bad molecules and so that shouldn't be impeded? Or is the system just gone awry a la` D Insipidus and not making enough Anti-Diuretic Hormone, so in that case the excess urination should be impeded?

Thanks again.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
The aspect of this topic that relates to the topic thread re metabolic acid and alkaline is that alcohol is very much alkaline-anaerobic-anabolic in character, and it is spectacularly effective at suppressing ketosis (fat-burning) pathways. It also produces NADH from both alcohol dehydrogenase and acetaldehyde dehydrogenase. If a particular person is already over-reduced and has low levels of NAD+ and NADP+, drinking alcohol could make this much worse. So I am concerned that these efffects can produce "ripples" in the cellular/mitochondrial energy pathways similar to what happens in alcoholics, who experience a "high" when NADH rises and a "crash" when NADH falls. So as long as they keep drinking, and fresh alcohol keeps the NADH "propped up," they postpone the crash. This "biochemical imperative" to keep drinking is the difference between social drinkers and alcoholic addiction.

This is very interesting, thank you.

Do you know whether exertion could have a similar effect, notably "a "high" when NADH rises and a "crash" when NADH falls"?

The reason I ask is that I, and others, I think, find that if we continue (over-) exerting, we seem to postpone the post-exertional malaise. However, the longer we keep overexerting, the worse the crash/PEM when we eventually stop.
 

Gondwanaland

Senior Member
Messages
5,095
polyuria in CFS, would it be wrong to try and reduce urine output? In other words, is the system getting rid of excess bad molecules and so that shouldn't be impeded? Or is the system just gone awry a la` D Insipidus and not making enough Anti-Diuretic Hormone, so in that case the excess urination should be impeded?
IME reversing excess acidity with oral magnesium oxide and sodium bicarbonate baths helped me to erradicate my polyuria. In addition, Saccharomyces boulardii helped in reducing histamine and vitamin A helped in solubilizing calcium.
My urine pH was 4.5 in the evening when I took my 1st bicarb bath. If I only knew it was that simple!